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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 閔明源(Ming-Yuan Min) | |
| dc.contributor.author | Yu-Wei Wu | en |
| dc.contributor.author | 吳玉威 | zh_TW |
| dc.date.accessioned | 2021-06-13T02:01:26Z | - |
| dc.date.available | 2008-07-20 | |
| dc.date.copyright | 2007-07-20 | |
| dc.date.issued | 2007 | |
| dc.date.submitted | 2007-07-06 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/30337 | - |
| dc.description.abstract | 橋腦中A7正腎上腺素神經核在痛覺傳遞的調控上扮演了很重要的角色，本論文為第一次對此正腎上腺素神經元所表現之A型鉀離子電流進行電生理、藥理特性及功能上的探討。此A型鉀離子電流活化閾值約在 -70 mV，半活化電位為-27.97 ± 1.71 mV，半不活化電位為 -72.31 ± 2.27 mV。此A型鉀離子電流從不活化回復非常快，在Vm = -100 mV時其回復時間長數為 21.87 ± 2.80 ms。對Kv4專一之抑制劑heteroprodotoxin2 (HpTx2)可顯著抑制此A型鉀離子電流，但是此電流不受到Kv3.4 專一之抑制劑 BDS-I所影響。此電流之生物物理及藥理特性結果顯示：A7正腎上腺素神經元之A型鉀離子電流是由Kv4次單元組成。以免疫組織化學染色方法發現Kv4.3鉀離子通道蛋白表現在A7正腎上腺素神經元之細胞本體及主要樹突上，顯示此A型鉀離子通道可能為Kv4.3所組成。此A型鉀離子通道不僅調控A7正腎上腺素神經元之動作電位的延遲產生及放射動作電位的瞬時頻率，更參與調控動作電位之寬度。實驗結果更進一步地證實：此A型鉀離子通道可被興奮性突觸後電位變化所活化，並可能在突觸訊號的傳遞與整合上扮演了重要的角色。此論文之研究結果讓我們對A7正腎上腺素神經元的電生理特性有更進一步的了解，對於A型鉀離子電流在痛覺的調控上也提供了一個可能的機制。 | zh_TW |
| dc.description.abstract | The pontine noradrenergic (NAergic) neurons located in A7 area are believed to play an important role in modulating nociception. This study provides the first functional analysis of the biophysical and pharmacological properties of A-type current (IA) in A7 NAergic neurons. IA in A7 NAergic neurons was activated at about -70 mV, with midpoint activation potential of -27.97 ± 1.71 mV. The midpoint inactivation potential was at about -72.31 ± 2.27 mV, and the recovery from inactivation was very quickly with a time constant of 21.87 ± 2.80 ms at Vm = -100 mV. The IA was sensitive to heteroprodotoxin2 (HpTx2), a Kv4 selective blocker, but not affected by BDS-I, a Kv3.4 selective blocker. These biophysical and pharmacological results demonstrated that A-type current in A7 NAergic neurons is mediated mainly by Kv4. By immunostaing, we found that Kv4.3 proteins were robustly expressed on the soma and dendrites. This result indicated that the A-type in A7 NAergic neurons may mediated by somatodendritic Kv4.3. This A-type current acted not only at subthreshold level to control the initiation of action potential and firing frequency, but was also activated at suprathreshold to shape the action potentials. Furthermore, it could be activated by membrane depolarization during excitatory synaptic transmission and might contribute to the synaptic signal propagation and integration in A7 NAergic neurons. These findings may help us understand more about the regulation of pain transmission. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-13T02:01:26Z (GMT). No. of bitstreams: 1 ntu-96-R94b41032-1.pdf: 2501988 bytes, checksum: a6a83de03967f5988ef77493c7310b79 (MD5) Previous issue date: 2007 | en |
| dc.description.tableofcontents | 口試委員審定書 I
致謝 II 中文摘要 IV Abstract V Contents VI Introduction 1 The ascending pain pathway and descending modulation of pain 1 The role of A7 catecholamine cell group in descending modulation of pain 2 The potassium channels overview 4 The voltage-gated K+ channels 4 The delayed-rectifier K+ channels 5 The A-type K+ channels 6 Objectives 9 Materials and Methods 11 Preparation of brain stem slices 11 Visualization of neurons in A7 area and whole cell patch clamp recording 11 Drugs 14 Data analysis 14 Filling recorded neurons with biocytin and immunohistochemistry 16 Immunohistochemistry for double labeling 17 Results 19 Identification and recording of NAergic neurons of A7 cell group in longitudinal brainstem slices 19 Prominent delay onset of action potential in DBH-ir neurons in the A7 cell group 20 Gating properties of IA evoked in DBH-ir neurons 22 The pharmacological profiles of IA evoked in DBH-ir neurons 24 The molecular composition of A-type potassium channels in DBH-ir neurons 25 The contribution of IA to the prominent delay in firing action potential 26 The contribution of IA to the firing frequency and action potential repolarization 27 Involvement of IA in the regulation of synaptic integration of DBH-ir neurons in A7 cell group 29 Discussions 31 Gating properties and molecular identity of IA in A7 NAergic neurons 31 Functional roles of Kv4.3 in A7 NAergic neurons 33 IA regulates the instant firing frequency in A7 NAergic neurons 34 IA regulates the spike shape in A7 NAergic neurons 35 IA regulates synaptic signal propagation and integration in A7 NAergic neurons 36 The physiological impacts of IA in A7 NAergic neurons in regulation of pain transmission 37 References 40 Table 49 Table.1 Gating properties of A-type potassium channels in A7 NAergic neurons 49 Figures 50 Fig 1. Identification and recording of A7 NAergic neurons in longitudinal brainstem slices 50 Fig 2. Prominent delay onset of action potential in A7 DBH-ir neurons 52 Fig 3. The peak amplitude and the charge density of IA in DBH-ir and non-DBH-ir neurons 53 Fig 4. The activation of IA evoked in DBH-ir neurons. 55 Figure 5. The steady-state inactivation of IA evoked in DBH-ir neurons. 56 Fig 6. The recovery from inactivation of IA evoked in DBH-ir neurons 57 Fig 7. The activation and inactivation of IA evoked in 50 mM TEA in DBH-ir neurons 58 Fig 8. The pharmacological properties of IA evoked in DBH-ir neurons – the response to 4-aminopyridine (4-AP) 60 Fig 9. The pharmacological properties of IA evoked in DBH-ir neurons - the response to BDS-I and Heteropodotoxin2 (HpTx2) 62 Fig 10. Molecular composition of A-type potassium channels in DBH-ir neurons. A1 and B1 63 Fig 11. The voltage dependence of delay onset of action potential in DBH-ir neurons 64 Fig 12. Contribution of IA to the prominent delay in firing action potential in DBH-ir neurons 65 Fig 13. Contribution of IA to the firing frequency in DBH-ir neurons 66 Fig. 14. Contribution of IA to the repolarization of action potential in DBH-ir neurons 67 Fig 15. Contribution of IA to the half-width of AHP in DBH-ir neurons 68 Fig 16. IA was activated during the interspike intervals in DBH-ir neurons 69 Fig 17. Evoked IA by subthreshold EPSP wave form in DBH-ir neurons 70 Fig 18. Increasing the stimulated response by 4-AP in DBH-ir neurons 71 | |
| dc.language.iso | en | |
| dc.subject | 全細胞記錄 | zh_TW |
| dc.subject | 腦幹 | zh_TW |
| dc.subject | A7核區 | zh_TW |
| dc.subject | 正腎上腺素 | zh_TW |
| dc.subject | A型鉀離子通道 | zh_TW |
| dc.subject | Kv4 | zh_TW |
| dc.subject | 痛覺傳導 | zh_TW |
| dc.subject | brainstem | en |
| dc.subject | whole-cell recording | en |
| dc.subject | pain transmission | en |
| dc.subject | A-type potassium channels | en |
| dc.subject | noradrenalin | en |
| dc.subject | A7 nucleus | en |
| dc.subject | Kv4 | en |
| dc.title | 大鼠A7核區兒茶酚胺神經細胞中A型鉀離子通道之功能探討 | zh_TW |
| dc.title | Functional Role of A-Type Potassium Channels in A7 Catecholamine Cell Group in Rats | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 95-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 楊琇雯,陳志成,連正章 | |
| dc.subject.keyword | 腦幹,A7核區,正腎上腺素,A型鉀離子通道,Kv4,痛覺傳導,全細胞記錄, | zh_TW |
| dc.subject.keyword | brainstem,A7 nucleus,noradrenalin,A-type potassium channels,Kv4,pain transmission,whole-cell recording, | en |
| dc.relation.page | 48 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2007-07-09 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 動物學研究研究所 | zh_TW |
| 顯示於系所單位： | 動物學研究所 | |
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